Carl June, via Getty

Carl June on CRISPR, CAR–T and how the Viet­nam War dropped him in­to med­i­cine

In Au­gust of 2011, Carl June and his team pub­lished a land­mark pa­per show­ing their CAR–T treat­ment had cleared a pa­tient of can­cer. A year-to-the-month lat­er, Jen­nifer Doud­na made an even big­ger splash when she pub­lished the first ma­jor CRISPR pa­per, set­ting off a decade of in­tense re­search and some­times even more in­tense pub­lic de­bate over the ethics of what the gene-edit­ing tool could do.

Last week, June, whose CAR–T work was even­tu­al­ly de­vel­oped by No­var­tis in­to Kym­ri­ah, pub­lished in Sci­ence the first US pa­per show­ing how the two could be brought to­geth­er. It was not on­ly one of the first time sci­en­tists have com­bined the ground­break­ing tools, but the first peer-re­viewed Amer­i­can pa­per show­ing how CRISPR could be used in pa­tients.

June used CRISPR to ed­it the cells of three pa­tients with ad­vanced blood can­cer, delet­ing the tra­di­tion­al T cell re­cep­tor and then eras­ing the PD–1 gene, a move de­signed to “un­leash” the im­mune cells. The ther­a­py didn’t cure the pa­tients, but the cells re­mained in the body for a me­di­an of 9 months, a ma­jor hur­dle for the ther­a­py.

End­points caught up with June about the long road both he and the field took to get here, if the treat­ment will ever scale up, and where CRISPR and oth­er ad­vance­ments can lead it.

The in­ter­view has been con­densed and edit­ed. 

You’ve spo­ken in the past about how you start­ed work­ing in this field in the mid-90s af­ter your wife passed away from can­cer. What were some of those ear­ly ef­forts? How did you start?

Well, I grad­u­at­ed from high school and had a low draft num­ber [for the Viet­nam War] and was go­ing to go to study en­gi­neer­ing at Stan­ford, but I was draft­ed and went in­to the Naval Acad­e­my in 1971, and I did that so I wouldn’t have to go to the rice fields.

The war end­ed in ’73, ’74, so when I grad­u­at­ed in 1975, I was al­lowed to go to med­ical school, and then I had a long term com­mit­ment to the Navy be­cause they paid for the Acadamy and Med­ical school. And I was in­ter­est­ed in re­search and at the time, what the Navy cared about was a small scale nu­clear dis­as­ter like in a sub­ma­rine, and like what hap­pened at Cher­nobyl and Fukushi­ma. So they sent me to the Fred  Hutchin­son Can­cer Cen­ter where I got trained in can­cer, as a med­ical on­col­o­gist. I was go­ing to open a bone mar­row trans­plant cen­ter in Bethes­da be­cause the Navy want­ed one in the event of a nu­clear cat­a­stro­phe.

And then in 1989, the Berlin Wall came down and there was no more Cold War. I had gone back to the Navy in ’86 for the trans­plant cen­ter, which nev­er hap­pened, so then I had to work in the lab full time. But in the Navy, all the re­search has to be about com­bat and ca­su­al­ty. They care about HIV, so my first pa­pers were on malar­ia and in­fec­tious dis­ease. And the first CAR-T tri­als were on HIV in the mid-90s.

David Porter

In ’96, my wife got di­ag­nosed with ovar­i­an can­cer and she was in re­mis­sion for 3-4 years. I moved to the Uni­ver­si­ty of Penn­syl­va­nia in 1999 and start­ed work­ing on can­cer be­cause I wasn’t al­lowed to do that with the Navy. My wife was ob­vi­ous­ly a lot of mo­ti­va­tion to do that. She passed away in 2001. Then I start­ed work­ing with David Porter on adop­tive trans­fer T cells.

I got my first grant to do CAR-T cells on HIV in 2004, and I learned a whole lot. I was lucky to have worked on HIV be­cause we did the first tri­als us­ing lentivirus­es, which is an en­gi­neered HIV virus.

I was trained in on­col­o­gy, and then be­cause of the Navy forced to work on HIV. It was ac­tu­al­ly a bless­ing in dis­guise.

So if you hadn’t been draft­ed, you would’ve be­come an en­gi­neer?

Yes. That’s what I was ful­ly in­tend­ing. My dad was a chem­i­cal en­gi­neer, my broth­er is an en­gi­neer. That’s what I thought I was go­ing to do. No one in my fam­i­ly was ever a physi­cian. It’s one of those many quirks of fate.

Back then, we didn’t have these ap­ti­tude tests. It was just hap­haz­ard. I ap­plied to three schools — Berke­ley, Stan­ford and Cal­tech — and I got in­to all three. It was just luck, fate.

And it turned out when I went to the Naval Acad­e­my, they had added a pre-med thing on­to the cur­ricu­lum the year be­fore, so that’s what I did when I start­ed, I did chem­istry.

I would’ve [oth­er­wise] been in nu­clear sub­marines. The most in­ter­est­ing thing in the Navy then was the nu­clear sub tech­nol­o­gy.

You talked about do­ing the first CAR-T tri­als on HIV pa­tients be­cause that’s where the fund­ing was. Was it al­ways in your head that this was even­tu­al­ly go­ing to be some­thing for can­cer?

So I got out of the Navy in ’99 and moved to Penn. I start­ed in ’98 work­ing on treat­ing leukemia, and then once I got to Penn, I con­tin­ued work­ing one day a week on HIV.

It’s kind of a Back-to-the-Fu­ture thing be­cause now can­cer has paved out a path to show that CAR–T cells can work and put down the man­u­fac­tur­ing and it’s go­ing to be a lot cheap­er mak­ing it for HIV. I still think that’s go­ing to hap­pen.

Jim Ri­ley, who used to be a post­doc in my lab, has some spec­tac­u­lar re­sults in mon­keys with HIV mod­els. They have a large NIH and NI­AID re­search pro­gram.

So we’re go­ing to see more and more of that. The CAR tech­nol­o­gy is go­ing to move out­side of can­cer, and in­to au­toim­mune and chron­ic in­fec­tions.

I want to jump over to cy­to­tox­ic re­lease syn­drome (CRS) be­cause a big part of the CRISPR study was that it didn’t pro­voke this po­ten­tial­ly dead­ly ad­verse ef­fect. When did you first be­come aware that CRS was go­ing to be a prob­lem?

I mean we saw it in the very first pa­tient we treat­ed but in all hon­esty, we missed it. I’m an MD, but I don’t see the pa­tient and David Porter took care of the first three pa­tients and our first pe­di­atric pa­tient, Emi­ly White­head.

In our first pa­tients, 2 out of 3, had com­plete re­mis­sion and there were fevers and it was CRS but we thought it was just an in­fec­tion, and we treat­ed with an­tibi­otics for 3 weeks and [even­tu­al­ly] it went away. And sort of mirac­u­lous­ly he was in re­mis­sion and is still in re­mis­sion, 9 years lat­er.

And then when we treat­ed Emi­ly. She was at a 106-de­gree fever over three days, and there was no in­fec­tion.

Tadamit­su Kishi­mo­to

I’ve told this sto­ry be­fore. My daugh­ter has rheuma­toid arthri­tis, and I had been pres­i­dent of the Clin­i­cal Im­mu­nol­o­gists So­ci­ety from 2009 to 2010, and the first good drug for ju­ve­nile rheuma­toid arthri­tis that came out. I was in­vit­ed to give the Japan­ese sci­en­tist Tadamit­su Kishi­mo­to the pres­i­den­tial award for in­vent­ing the drug.

Then in 2012, Emi­ly White­head was lit­er­al­ly dy­ing from CRS, she had mul­ti­ple or­gan fail­ures. And her labs came back and IL-6 lev­els were 1000x nor­mal. It turns out the drug I was look­ing at for my daugh­ter, it blocks IL-6 lev­els. I called the physi­cian and I said, ‘lis­ten there’s some­thing ac­tion­able here, since it’s in your for­mu­la­ry to give it to her off-la­bel.’

And she gave her the ap­pro­pri­ate dose for rheuma­toid arthri­tis. It was mirac­u­lous. She woke up very rapid­ly.

Now it’s co-la­beled. When the FDA ap­proved Kym­ri­ah, it was co-la­beled. It kind of saved the field.

How were you feel­ing dur­ing this time? Did you have any idea what was hap­pen­ing to her?

No, not un­til we got the cy­tokine lev­els, and then it was re­al­ly clear. The cy­tokine lev­els go up and it ex­act­ly co­in­cid­ed. Then we retroac­tive­ly checked out adults and they had ad­verse re­ac­tions and it easy to see. We hadn’t been on the look­out be­cause it wasn’t in our mouse mod­els.

And it ap­peared with those who got cured. It’s one of the first on-tar­get tox­i­c­i­ties seen in can­cer, a tox­i­c­i­ty that hap­pens when you get bet­ter. All the tox­i­c­i­ties from chemother­a­py are off-tar­get: like leukope­nia or hair loss.

I had a physi­cian who had a fever of 106,  I saw him on a fever when he was start­ing to get CRS. When the nurse came in and it said 106, they thought the ther­mome­ter must be bro­ken. On Mon­day, I saw him, and said “how are you feel­ing” and he said “fine.” And I looked at the ther­mome­ter and his tem­per­a­ture was still 102.

Peo­ple will will­ing­ly tol­er­ate on-tar­get tox­i­c­i­ty — that’s very dif­fer­ent from chemother­a­py — if they know it helps get them bet­ter. That’s a new prin­ci­ple in can­cer ther­a­py.

You had these ear­ly CAR–T re­sults al­most at the same time that Doud­na pub­lish­es the first CRISPR pa­pers, then still in bac­te­ria. When did you first start think­ing about com­bin­ing the two?

Yeah, it was pub­lished in Sci­ence in 2012 and that’s when Emi­ly White­head got treat­ed. It’s an amaz­ing thing.

That’s some­thing so or­thog­o­nal. You think ‘how in the heck can that ever ben­e­fit CAR–T cells?׳ but my lab had done the first edit­ed cells in pa­tients, pub­lished in 2012. And we used zinc-fin­gered nu­cle­as­es, which were the pre­de­ces­sors to CRISPR. It knocked out one gene at a time, but we showed it was safe.

I was al­ready in­to gene edit­ing be­cause it could make T cells re­sis­tant to HIV. So it was pret­ty ob­vi­ous that there were can­di­dates in T cells that you can knock out. And al­most every lab start­ed work­ing on some with CRISPR, cause it was much eas­i­er.

We were the first to get full ap­proval by the FDA, so we worked on it from 2012, had all the pre­clin­i­cal da­ta by 2016, and then it takes a while to de­vel­op a lot of new as­says for this as we were very cau­tious to op­ti­mize safe­ty and it took longer than we want­ed, but in the end, we learned a tremen­dous amount.

So what did we learn?

First of all our pa­tients had ad­vanced metasta­t­ic can­cer and had had a lot of chemother­a­py. The first pa­tient had had 3 bone mar­row trans­plants.

One thing is fea­si­bil­i­ty: could you re­al­ly do all the com­plex en­gi­neer­ing? So we found out we could. fea­si­bil­i­ty was passed.

An­oth­er was the fact that cas9 came out of bac­te­ria, forms of strep and staph. Every­one has pre-ex­ist­ing im­mu­ni­ty to Cas9 and we had ex­pe­ri­ence from the first tri­al with Sang­amo [with zinc-fin­ger nu­cle­as­es] where some pa­tients had a very high fever. In that case, we had used ade­n­ovirus­es, and it turned out our pa­tients had very high lev­els of base­line im­mune re­sponse to ade­n­ovirus­es, so we were wor­ried that would hap­pen with CRISPR, and it did not hap­pen.

It did not have any tox­i­c­i­ty. If it had, it would have re­al­ly set the field back. If there was an im­mune re­sponse to cas9 and CRISPR, there could’ve been a re­al bar­ri­er to the field.

And then, the cells sur­vived in the pa­tients. The fur­thest on, it was 9 months. The cells had a very high lev­el of sur­vival. In the pre­vi­ous tri­als, the cells sur­vived less than 7 days. In our case, the half-life was 85 days. We don’t know the mech­a­nism yet.

And we found very big pre­ci­sion in the mol­e­c­u­lar scis­sors, and that was a good thing for the field. You could cut 3 dif­fer­ent genes on 3 dif­fer­ent chro­mo­somes and have such high fi­deli­ty.

It [CRISPR] is liv­ing up to the hype. It’s go­ing to fix all these dis­eases.

What’s the po­ten­tial in CAR-T, specif­i­cal­ly?

Well there’s many many genes that you can add. There are many genes that knock­ing out will make the cells work bet­ter. We start­ed with the cell re­cep­tor. There are many, I think, aca­d­e­mics and biotechs do­ing this now and it should make the cells more po­tent and less tox­ic.

And more broad­ly, what else are you look­ing at for the fu­ture of CAR–T? The week be­fore your pa­per, there were the re­sults from MD An­der­son on nat­ur­al killer cells. 

Dif­fer­ent cell types, nat­ur­al killer cells, stem cells — putting CAR mol­e­cules in­to stem cells, macrophages. One of my grad­u­ate stu­dents start­ed a com­pa­ny to do CAR macrophages and macrophages ac­tu­al­ly eat tu­mor cells, as op­posed to T cells that punch holes in them.

There will be dif­fer­ent cell types and there will be many more ways to ed­it cells. The prime edit­ing and base edit­ing. All dif­fer­ent new vari­a­tions.

You’ve talked about how peo­ple used to think the im­muno-on­col­o­gy, if it ever worked, would nev­er­the­less be a bou­tique treat­ment. De­spite all the ad­vance­ments, No­var­tis and Gilead still have not met the sales they once hoped to grab from their CAR–T treat­ments. Are you con­fi­dent CAR–T will ever be wide­ly ac­ces­si­ble?

Oh yeah, No­var­tis’ sales are go­ing up. They had a hic­cup launch­ing.

Back in ’96 or ’97, when Genen­tech launched Her­ceptin, their com­mer­cial an­ti­body, they couldn’t meet the de­mand ei­ther and then they scaled up and learned how to do bet­ter cul­tures. So right now No­var­tis is us­ing tech in­vent­ed in my lab in the 1990s cul­ture tech that’s com­plex and re­quires a lot of la­bor, so the most ex­pen­sive part is hu­man la­bor. A lot can be made ro­bot­ic. The scale prob­lem will be much eas­i­er.

That’s an en­gi­neer­ing prob­lem that will be­come a thing of the past. The man­u­fac­tur­ing prob­lem will get a lot cheap­er. Here in the US, we have a huge prob­lem with how drugs are priced. We have a prob­lem with pric­ing. That’s a po­lit­i­cal is­sue.

But in cell ther­a­py, it’s just kind of the growth things you see in a new in­dus­try. It’ll get worked out.

This ar­ti­cle has been up­dat­ed to re­flect that Jim Ri­ley con­duct­ed work on CAR in HIV.  

Lessons for biotech and phar­ma from a doc­tor who chased his own cure

After being struck by a rare disease as a healthy third year medical student, David Fajgenbaum began an arduous journey chasing his own cure. Amidst the hustle of this year’s JP Morgan conference, the digital trials platform Medable partnered with Endpoints Studio to share Dr. Fajgenbaum’s story with the drug development industry.

What follows is an edited transcript of the conversation between Medable CEO Dr. Michelle Longmire and Dr. Fajgenbaum, and it is full of lessons for biotech executives charged with bringing the next generation of medicines to patients.

Kathy High (file photo)

Gene ther­a­py pi­o­neer Kathy High has left Spark af­ter com­plet­ing $4.3B union with Roche

Kathy High dedicated the past seven years of her life shepherding experimental gene therapies she’s developed at Children’s Hospital of Philadelphia toward the market as president and head of R&D at Spark Therapeutics. Now that the biotech startup is fully absorbed into Roche — with an FDA approval, a $4.3 billion buyout and a promising hemophilia program to boast — she’s ready to move on.

Roche confirmed her departure with Endpoints News and noted “she will take some well-deserved time off and then will begin a new chapter in a sabbatical at a university.”

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Deborah Dunsire

The fourth CGRP mi­graine drug is here. Time for Lund­beck to prove it's worth $2B

They may be late, but Lundbeck is now officially in the game for preventing migraine with CGRP drugs.

The FDA has OK’d eptinezumab, the prize in Lundbeck’s $2 billion acquisition of Alder. Like rival offerings from Amgen/Novartis, Eli Lilly and Teva, the antibody blocks the calcitonin gene-related peptide, which is believed to dilate blood vessels in the brain and cause pain.

It will now be sold as Vyepti. The company has yet to announce a price. Amgen and Novartis had set the wholesale acquisition cost of their pioneering Aimovig at $6,900 for a year’s supply before raising it slightly this year; Lilly and Teva had followed suit with Emgality and Ajovy.

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Tal Zaks (Moderna via YouTube)

For two decades, a new vac­cine tech­nol­o­gy has been slow­ly ap­proach­ing prime time. Now, can it stop a pan­dem­ic?

Two months before the outbreak, Moderna CMO Tal Zaks traveled from Cambridge, MA to Washington DC to meet with Anthony Fauci and the leaders of the National Institutes of Health.

For two years, Moderna had worked closely with NIH researchers to build a new kind of vaccine for MERS, one of the deadliest new viruses to emerge in the 21st century. The program was one test for a new technology designed to be faster, cheaper and more precise than the ways vaccines had been made for over a century. They had gathered evidence the technology could work in principle, and Fauci, the longtime head of the National Institute of Allergy and Infectious Diseases and a longtime advocate for better epidemic preparedness, wanted to see if it, along with a couple of other approaches, could work in a worst-case scenario: A pandemic.

“[We were] trying to find a test case for how to demonstrate if our technology could rapidly prepare,” Zaks told Endpoints News.

Zaks and Fauci, of course, wouldn’t have to wait to develop a new test. By year’s end, an outbreak in China would short circuit the need for one and throw them into 24/7 work on a real-world emergency. They also weren’t the only ones with new technology who saw a chance to help in a crisis.

An ocean away, Lidia Oostvogels was still on vacation and relaxing at her mother’s house in Belgium when her Facebook started changing. It was days after Christmas and on most people’s feeds, the news that China had reported a novel virus to the World Health Organization blurred into the stream of holiday sweaters and fir trees. But on Oostvogels’s feed, full of vaccine researchers and virus experts, speculation boiled: There was a virus in China, something contained to the country, but “exotic,” “weird,” and maybe having to do with animals. Maybe a coronavirus.

Lidia Oostvogels

“I was immediately thinking like, ‘Hey, this is something that if needed, we can play a role,'” Oostvogels told Endpoints.

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Tim Mayleben (file photo)

Es­pe­ri­on's goldilocks cho­les­terol fight­er wins FDA ap­proval — will its 'tra­di­tion­al' pric­ing ap­proach spur adop­tion?

It’s more effective than decades-old statins but not as good as the injectable PCSK9 — the goldilocks treatment for cholesterol-lowering, bempedoic acid, has secured FDA approval.

Its maker, Esperion Therapeutics, is betting that their pricing strategy — a planned list price of between $10 to $11 a day — will help it skirt the pushback the PCSK9 cholesterol fighters, Repatha and Praluent, got from payers for their high sticker prices.

The sky-high expectations for the pair of PCSK9 drugs that were first approved in 2015 quickly simmered — and despite a 60% price cut, coupled with data showing the therapies also significantly cut cardiovascular risk, sales have not really perked up.

Esperion is convinced that by virtue of being a cheaper oral therapy, bempedoic acid will hit that sweet spot in terms of adoption.

“We’re kind of like the old comfortable shoe,” Esperion’s chief commercial officer Mark Glickman remarked in an interview with Endpoints News ahead of the decision date. “It’s an oral product, once-daily and nontitratable — these are things that just resonate so true with patients and physicians and I think we’ve kind of forgotten about that.”

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James Collins, Broad Institute via Youtube

UP­DAT­ED: A space odyssey for new an­tibi­otics: MIT's ma­chine learn­ing ap­proach

Drug development is complex, expensive and comes with lousy odds of success — but in most cases, if you make it across the finish line brandishing a product with an edge (and play your cards right) it can be a lucrative endeavor.

As it stands, the antibiotic market is cursed — it harbors the stink of multiple bankruptcies, a dearth of innovation, and is consequently barely whetting the voracious appetites of big pharma or venture capitalists. Enter artificial intelligence — the biopharma industry’s cure-all for the pesky process of making a therapeutic, including data mining, drug discovery, optimal drug delivery, and addressable patient population.

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Gilead los­es two more patent chal­lenges on HIV pill, set­ting up court­room fight in Delaware

Gilead sustained two more losses in their efforts to rid themselves of an activist-backed patent lawsuit from the US government over a best-selling HIV pill.

Urged on by activists seeking to divert a portion of Gilead’s revenue to clinics and prevention programs, the Department of Health and Human Services made a claim to some of the patents for the best-selling HIV prevention drug, Truvada, also known as PrEP. Gilead responded by arguing in court that HHS’s patents were invalid.

Today, the US Patent and Trademark Office ruled that Gilead was likely to lose the last two of those challenges as well. The USPTO ruled against Gilead on the first two patents earlier this month.

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Christos Kyratsous (via LinkedIn)

He built a MERS treat­ment in 6 months and then the best Ebo­la drug. Now Chris­tos Kyrat­sous turns his sights on Covid-19

TARRYTOWN, NY — In 2015, as the Ebola epidemic raged through swaths of West Africa, Kristen Pascal’s roommates sat her down on their couch and staged an intervention.

“Are you sure this is what you want to be doing with your life?” she recalls them asking her.

Special report

Pascal, a research associate for Regeneron, had been coming home at 2 am and leaving at 6 am. At one point, she didn’t see her roommate for a week. For months, that was life in Christos Kyratsous’ lab as the pair led a company-wide race to develop the first drug that could effectively treat Ebola before the outbreak ended. For Pascal, that was worth it.

“I’m ok, I don’t have Ebola,” Pascal told them. “I see that death toll rising and I can’t not do something about it.”

Last August, Regeneron learned they had succeeded: In a large trial across West Africa, their drug, REGN-EB3, was vastly more effective than the standard treatments. It was surprise news for the company, coming just 10 months into a trial they thought would take several years and a major victory in the global fight against a deadly virus that killed over 2,000 in 2019 and can carry a mortality rate of up to 90%.

For Kyratsous and Pascal, though, it brought only fleeting reprieve. Just four months after the NIH informed them REGN-EB3 worked, Kyratsous was back in his office reading the New York Times for updates on a new outbreak on another continent, and wondering alongside Pascal and senior management whether it was time to pull the trigger again.

In late January, as the death toll swelled and the first confirmed cases outside China broke double digits, they made a decision. Soon they were back on the phone with the multiple government agencies and their coronavirus partners at the University of Maryland’s Level 3 bio lab. The question was simple: Can Kyratsous and his team use a process honed over two previous outbreaks, and create a treatment before the newest epidemic ends? Or worse, if, as world health experts fear, it doesn’t vanish but becomes a recurrent virus like the flu?

“Christos likes things immediately,” Matt Frieman, Regeneron’s coronavirus collaborator at the University of Maryland, told Endpoints. “That’s what makes us good collaborators: We push each other to develop things faster and faster.”

Kristen Pascal (Regeneron)

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The first time Regeneron tried to respond to a global outbreak, it was something of a systems test, Kyratsous explains from his office at Regeneron’s Tarrytown headquarters. Kyratsous, newly promoted, has crammed it with photos of his family, sketches of viral vectors and a shark he drew for his 3-year-old son. He speaks rapidly – an idiosyncrasy his press person says has only been aggravated this afternoon by the contents of his “Regeneron Infectious Diseases”-minted espresso glass – and he gesticulates with similar fluidity, tumbling through antibodies, MERS, the novel coronavirus, Ebola-infected monkeys.

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Bank­rupt an­tibi­otics mak­er Ar­a­digm turns to old part­ner/in­vestor for fi­nal $3M fire sale

Grifols once paid Aradigm $26 million for a stake in its inhaled antibiotics. But with Aradigm now in bankruptcy, the Spanish drugmaker is dishing out a final $3.2 million to buy it all.

The fire sale — which comes one year after Aradigm filed for Chapter 11 following a regulatory trifecta for disaster — will see Grifols obtain assets and IP to Apulmiq (formerly Pulmaquin and Linhaliq in Europe), Lipoquin and free ciprofloxacin. In addition to waiving its claims in the bankruptcy case, Grifols also agreed to milestone payments up to $3 million more upon any regulatory approvals.